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Bonadonna, R. C.

Publications and source records attributed to Bonadonna, R. C..

2 recordsLinked to original sources

A novel cell indirect calorimetry method unveils the metabolic fluxomic signatures of human monocyte derived M(LPS+INF-γ) and M(IL-4) macrophages

Macrophages (M{Phi}) display distinct immunometabolic phenotypes upon polarization. While transcriptomic analyses have suggested divergent metabolic programs in human M(LPS+INF-{gamma}) and M(IL-4) M{Phi}, a comprehensive assessment of their metabolic fluxes is lacking. Aim of this study is to 1. develop and validate a novel indirect microcalorimetry method for quantifying cellular metabolic fluxes, and 2. exploit it to characterize fluxomic signatures of polarized human monocyte-derived macrophages. MethodsM{Phi} from healthy donors were differentiated into M0, M(LPS+INF-{gamma}), and M(IL-4) phenotypes and studied in four defined media: substrate-free, glucose, glycyl-glutamine, and glucose + glycyl-glutamine. A steady-state fluxomic model was constructed by integrating four independent measures - oxygen consumption and proton production (Seahorse XFp), lactate and ammonia release (microfluorimetry) - into stoichiometric equations of metabolism (SAAM II software). ResultsFluxes revealed that macrophages rely on glucose to sustain glycolysis, contributing [~]30% of citrate synthase flux, and predominantly on lipids for net citrate synthesis (first step of Krebs cycle). Upon polarization, M(LPS+INF-{gamma}) macrophages showed increased anaerobic glycolysis versus M0 and M(IL-4), with similar TCA fluxes to M0. In contrast, M(IL-4) macrophages exhibited higher TCA and malic enzyme fluxes, especially with glucose and glycyl-glutamine, and a trend toward enhanced lipid oxidation. ConclusionsThis novel method enables precise quantification of bioenergetic fluxes. In human M{Phi}, it reveals that M(LPS+INF-{gamma}) and M(IL-4) subsets exhibit distinct metabolic phenotypes, consistent with their immunological roles. These results resolve transcriptomic-metabolic discrepancies and provide a robust framework for assessing immunometabolism in primary human cells.

physiology↗

Loss of ZnT8 function protects against diabetes by enhanced insulin secretion

A rare loss-of-function variant p.Arg138* in SLC30A8 encoding the zinc transporter 8 (ZnT8) enriched in Western Finland protects against type 2 diabetes (T2D). We recruited relatives of the identified carriers and showed that protection was associated with better insulin secretion due to enhanced glucose responsiveness and proinsulin conversion, especially compared with individuals matched for the genotype of a common T2D risk variant in SLC30A8, p.Arg325. In genome-edited human IPS-derived {beta}-like cells, we establish that the p.Arg138* variant results in reduced SLC30A8 expression due to haploinsufficiency. In human {beta}-cells loss of SLC30A8 leads to increased glucose responsiveness and reduced KATP channel function, which was also seen in isolated islets from carriers of the T2D-protective allele p.Trp325. These data position ZnT8 as an appealing target for treatment aiming at maintaining insulin secretion capacity in T2D.

genetics↗